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TGF-h1-mediated activations of c-Src and Rac1 modulate levels of cyclins
Cited 30 time in
Web of Science
Cited 30 time in Scopus
- Authors
- Issue Date
- 2005
- Publisher
- Elsevier
- Citation
- Biochim. Biophys. Acta 1743 (2005) 151– 161
- Abstract
- Integrin-mediated cell adhesion transduces signals to regulate actin cytoskeleton and cell proliferation. While understanding how integrin
signals cross-talk with the TGF-h1 pathways, we observed lamellipodia formation and cyclin regulation in Hep3B cells, following TGF-h1
treatment. To answer if integrin signaling via actin organization might regulate cell cycle progression after TGF-h1 treatment, we analyzed
cross-talk between the two receptor-mediated pathways in hepatoma cells on specific ECMs. We found that basal and TGF-h1-mediated
activation of c-Src and Rac1, expression of cyclins E and A, and suppression of p27Kip1 were significant in cells replated on fibronectin, but
not in cells on collagen I, indicating a different integrin-mediated cellular response to TGF-h1 treatment. Levels of tyrosine phosphorylation
and actin-enriched lamellipodia on fibronectin were also more prominent than in cells on collagen I. Studies using pharmacological inhibitors
or transient transfections revealed that the preferential TGF-h1 effects in cells on fibronectin required c-Src family kinase activity. These
observations suggest that a specific cross-talk between TGF-h1 and fibronectin-binding integrin signal pathways leads to the activation of c-
Src/Rac1/actin-organization, leading to changes in cell cycle regulator levels in hepatoma cells. Therefore, this study represents another
mechanism to regulate cell cycle regulators when integrin signaling is collaborative with TGF-h1 pathways.
- ISSN
- 0167-4889
- Language
- English
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